Cited by 115Pancreatic function and diabetesMitochondrial Function and PathologyDiabetes and associated disorders

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PDX1 Deficiency Causes Mitochondrial Dysfunction and Defective Insulin Secretion through TFAM Suppression

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Gauthier, Benoit R., Wiederkehr, Andreas, Baquié, Mathurin, Dai, Chunhua, Powers, Alvin C., Kerr-Conte, Julie, Pattou, François, MacDonald, Raymond J., Ferrer, Jorge, Wollheim, Claes B.·2009·Cell Metabolism

DOI 10.1016/j.cmet.2009.07.002PMC PMC4012862

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Abstract

Mutations in the transcription factor Pdx1 cause maturity-onset diabetes of the young 4 (MODY4). Islet transduction with dominant-negative Pdx1 (RIPDN79PDX1) impairs mitochondrial metabolism and glucose-stimulated insulin secretion (GSIS). Transcript profiling revealed suppression of nuclear-encoded mitochondrial factor A (TFAM). Herein, we show that Pdx1 suppression in adult mice reduces islet TFAM expression coinciding with hyperglycemia. We define TFAM as a direct target of Pdx1 both in rat INS1 cells and human islets. Adenoviral overexpression of TFAM along with RIPDN79PDX1 in isolated rat islets rescued mitochondrial DNA (mtDNA) copy number and restored respiratory chain activity as well as glucose-induced ATP synthesis and insulin secretion. CGP37157, which blocks the mitochondrial Na(+)/Ca(2+) exchanger, restored ATP generation and GSIS in RIPDN79PDX1 islets, thereby bypassing the transcriptional defect. Thus, the genetic control by the beta cell-specific factor Pdx1 of the ubiquitous gene TFAM maintains beta cell mtDNA vital for ATP production and normal GSIS.

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Authors: Gauthier, B. R., Wiederkehr, A., Baquié, M., Dai, C., Powers, A. C., Kerr-Conte, J., Pattou, F., MacDonald, R. J., Ferrer, J., & Wollheim, C. B.
Affiliations: University of Geneva (CH)
Vanderbilt University (US)
Inserm (FR)
The University of Texas Southwestern Medical Center (US)
Hospital Clínic de Barcelona (ES)
Corresponding author: Gauthier, Benoit R.
ORCID: Gauthier, Benoit R.
Wiederkehr, Andreas
Dai, Chunhua
Powers, Alvin C.
Kerr-Conte, Julie
Pattou, François
MacDonald, Raymond J.
Ferrer, Jorge
Wollheim, Claes B.
Venue: Cell Metabolism
Publisher: Elsevier BV
Published: 2009-08
Volume: 10
Issue: 2
Pages: 110-118
ISSN: 1550-4131 (ISSN-L)
DOI: 10.1016/j.cmet.2009.07.002
PMC: PMC4012862
OpenAlex: W2061113221
Cited by: 115
References: 41
Citations by year: 2026: 3 · 2025: 6 · 2024: 3 · 2023: 5 · 2022: 10 · 2021: 4 · 2020: 6 · 2019: 8 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 11 · 2014: 7 · 2013: 2 · 2012: 10
FWCI: 5.16
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1446 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Cell Metabolism (publishedVersion)
PubMed (publishedVersion)
Archive ouverte UNIGE (University of Geneva) (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders: National Institutes of Health (DK20593, DK68854, DK69603)
Juvenile Diabetes Research Foundation International
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (310000-116750/1, 310030-119763, 32-66907.01, LSHM-CT-2006-518153)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords: PDX1, TFAM, mitochondrial dysfunction, insulin secretion, glucose-stimulated insulin secretion, pancreatic beta cells, mitochondrial DNA copy number, electron transport chain, ATP production, mitochondrial Na+/Ca2+ exchanger, hyperglycemia, islets
MeSH terms: Insulin Secretion, Animals, Base Sequence, DNA-Binding Proteins, Doxycycline, Glucose, High Mobility Group Proteins, Humans, Insulin, Islets of Langerhans, Male, Mice, Transgenic, Mitochondria, Promoter Regions, Genetic, Transcription Factors, Trans-Activators, Rats, Wistar, Homeodomain Proteins, Sodium-Calcium Exchanger, Mitochondrial Proteins, Mice, Rats

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PDX1 Deficiency Causes Mitochondrial Dysfunction and Defective Insulin Secretion through TFAM Suppression

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